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Characterization of the 17p amplicon in human sarcomas: Microsatellite marker analysis
Author(s) -
Wolf Maija,
Tarkkanen Maija,
Hulsebos Theo,
Larramendy Marcelo L.,
Forus Anne,
Myklebost Ola,
Aaltonen Lauri A.,
Elomaa Inkeri,
Knuutila Sakari
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990730)82:3<329::aid-ijc4>3.0.co;2-1
Subject(s) - microsatellite , loss of heterozygosity , amplicon , biology , comparative genomic hybridization , southern blot , sarcoma , cytogenetics , microbiology and biotechnology , genetics , allele , polymerase chain reaction , pathology , gene , chromosome , medicine
The structure of the 17p amplicon from 9 human sarcoma specimens evaluated by comparative genomic hybridization (CGH) has been studied by analyzing 28 microsatellite markers by PCR. Eleven sarcoma specimens showing no DNA copy number increases at 17p by CGH were analyzed as control samples. Five specimens were analyzed by Southern blotting using probes that have previously shown amplification at the 17p12 region in astrocytoma and high‐grade osteosarcoma samples. Microsatellite marker analyses revealed that all samples but 1 showing copy number increases at 17p by CGH displayed allelic imbalance that confirmed the CGH findings. Seven of these 9 cases displayed gain in copy number by microsatellite marker analysis. Four cases displaying gain in copy number were associated with loss of heterozygosity at other loci. Southern blot analysis showed amplification in 3 cases, all of them had shown copy number increases by CGH and microsatellite marker analysis, except one case, which was not included in the microsatellite marker analysis. Our results reveal the complexity of the 17p amplicon in sarcomas, suggesting that multiple target genes are involved in tumorigenesis. Int. J. Cancer 82:329–333, 1999. © 1999 Wiley‐Liss, Inc.